Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Apr 30;10:942. doi: 10.3389/fimmu.2019.00942

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2019 Popugailo, Rotfogel, Supper, Hillman and Kaempfer.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Superantigen binds directly into the homodimer interfaces of CD28 and B7-2, triggering B7-2/CD28 engagement that induces an inflammatory cytokine storm. Schematic diagram showing the interaction of a superantigen, SMEZ, with CD28 on the T cell and B7-2 on the antigen-presenting cell (APC). For clarity, the second monomer in the CD28 homodimer and engagement by SMEZ of TCR and MHC-II molecule were omitted. (A) Formation of the B7-2/CD28 costimulatory axis enables expression of inflammatory cytokines. (B) Two superantigen molecules bind, through their accessible β-strand(8)/hinge/α-helix(4) domain (magenta), B7-2 and CD28 at their homodimer interfaces within the extracellular domains. Binding of the superantigen potently enhances B7-2/CD28 engagement and inflammatory signaling.